Smeets J L, Allessie M A, Lammers W J, Bonke F I, Hollen J
Circ Res. 1986 Jan;58(1):96-108. doi: 10.1161/01.res.58.1.96.
We measured the wavelength of the cardiac impulse, defined as the distance traveled by the depolarization wave during the functional refractory period, in isolated narrow strips of rabbit atrium. During control, wavelength was 42 mm during pacing with 2 Hz, and was 28 mm at the maximum pacing rate; early premature beats had a wavelength as short as 23 mm. Administration of carbamylcholine (4 X 10(-7) g/ml) shortened the wavelength to 21 mm during 2 Hz, 18 mm at the maximum pacing rate Fmax, and 16 mm during an early premature impulse, respectively. The effects of epinephrine (6 X 10(-7) M) were strongly rate dependent. At slow heart rates, epinephrine clearly prolonged the wavelength (58 mm), whereas, during maximum pacing, wavelength remained unchanged (28 mm). Hypokalemia (2 mM) decreased the length of the impulse at all stimulation frequencies. Moderate hyperkalemia (5.6 and 7.0 mM) did not modify wavelength because refractoriness and conduction velocity were affected proportionally. Above 7.0 mM potassium, the wavelength became progressively prolonged because of the development of post-repolarization refractoriness. Cooling to 27 degrees C resulted in a slight lengthening of the impulse. At lower temperatures, however, wavelength prolonged significantly because of a relatively strong prolongation of the refractory period. In separate experiments in 15 X 20 mm segments of atrium, reentrant tachyarrhythmias were induced and the circuit size compared with the wavelength. The size of intraatrial circuits was similar to the magnitude of the measured wavelength during maximum pacing. Carbamylcholine and hypokalemia, both of which shorten the impulse length, also clearly decreased the size of reentrant circuits. Cooling to 27 degrees C, which affects both refractoriness and conduction velocity, only slightly prolonged the wavelength; accordingly, the size of reentrant circuits at 27 degrees C was only slightly longer than at 37 degrees C. These experiments emphasize the importance of the wavelength of the cardiac impulse in relation to the occurrence of intramyocardial reentry.
我们在离体的兔心房窄条组织中测量了心脏冲动的波长，心脏冲动的波长定义为去极化波在功能性不应期内传播的距离。在对照期间，以2赫兹起搏时波长为42毫米，在最大起搏频率时为28毫米；早期早搏的波长短至23毫米。给予氨甲酰胆碱（4×10⁻⁷克/毫升）后，在2赫兹时波长缩短至21毫米，在最大起搏频率Fmax时为18毫米，在早期早搏冲动时为16毫米。肾上腺素（6×10⁻⁷摩尔）的作用强烈依赖于心率。在心率缓慢时，肾上腺素明显延长波长（58毫米），而在最大起搏时，波长保持不变（28毫米）。低钾血症（2毫摩尔）在所有刺激频率下均缩短冲动长度。中度高钾血症（5.6和7.0毫摩尔）未改变波长，因为不应期和传导速度受到成比例的影响。钾浓度高于7.0毫摩尔时，由于复极化后不应期的出现，波长逐渐延长。冷却至27摄氏度导致冲动略有延长。然而，在较低温度下，由于不应期相对强烈的延长，波长显著延长。在15×20毫米的心房节段进行的单独实验中，诱发了折返性快速心律失常，并将折返环大小与波长进行比较。心房内折返环的大小与最大起搏时测量的波长大小相似。氨甲酰胆碱和低钾血症均缩短冲动长度，也明显减小了折返环的大小。冷却至27摄氏度会影响不应期和传导速度，仅使波长略有延长；因此，27摄氏度时折返环的大小仅比37摄氏度时略长。这些实验强调了心脏冲动波长与心肌内折返发生的关系的重要性。
